Baroreflex control of stroke volume in man: an effect mediated by the vagus

Abstract

1. Beat-by-beat changes in cardiac performance in response to arterial baroreceptor stimulation induced by phenylephrine were evaluated by pulsed-wave aortic Doppler ultrasound in eighteen subjects. Stroke distance was used as an index of stroke volume and minute distance as an index of cardiac output; peak velocity was also measured. 2. The sensitivity of the baroreceptor-cardiac reflex was assessed by calculating the slope of the regression lines relating the changes in heart period (R-R interval), peak velocity and stroke distance in response to the rise in systolic blood pressure (SBP) induced by phenylephrine. In ten subjects the experiment was repeated after vagal blockade by atropine. Since the tachycardia induced by vagal blockade could alter the sensitivity of the baroreflex, we compared the results obtained after atropine with those obtained during pacing at similar rates in six subjects with cardiac pacemakers. 3. As R-R interval lengthened in response to the rise in SBP, stroke distance and peak velocity fell sharply. The subjects with a highly sensitive baroreceptor-heart rate reflex showed the greatest fall in peak velocity and stroke distance. The slope of the relationship between R-R interval and SBP for each subject correlated closely with that of peak velocity/SBP (correlation coefficient, r = 0.88) and stroke distance/SBP (r = 0.93) relationships. 4. Atropine virtually abolished all the cardiac reflex changes, despite a considerable increase in SBP induced by phenylephrine. At comparable heart rates achieved by pacing the sensitivity of the baroreceptor-cardiac reflex (calculated from the slopes of the regression lines relating changes in stroke distance and in peak velocity to the rise in SBP) was maintained and was significantly greater when compared to that obtained after vagal blockade. 5. These results show that the stimulation of arterial baroreceptors is accompanied by a fall in the Doppler-derived indices of stroke volume and cardiac output. This response is neural and is abolished by atropine, which indicates that it is mediated through the efferent vagus.